Search

OBJECTIVE: The purpose of this report is to describe the relationship between the renal artery and the azygos vein in patients with congenital infrahepatic interruption of the inferior vena cava with azygos continuation. CONCLUSION: Using abdominal sonography, we showed that in patients with interruption of the inferior vena cava with azygos continuation, the renal artery is ventral to the azygos vein. Because this malformation is frequently associated with cardiac and situs anomalies, awareness of the anatomic relationship between the renal artery and the azygos vein can aid in diagnosis and may substitute for more expensive and invasive diagnostic procedures.

Treatment of HIV-infected patients has come a long way since the not-so-long-ago beginning of the AIDS epidemic. Implementation of new drug therapies has increased longevity of a patient's life after being diagnosed with the virus. Because HIV-related illnesses are consequently becoming more chronic in nature, patients commonly experience potentially debilitating CNS, PNS, or musculoskeletal problems during the course of the disease. As a result, these patients require delicate care from a number of different health care providers. A multidisciplinary team approach must be used within the podiatrist's treatment regimen. This team must include the physiatrist overseeing the physical therapist, to provide complete and optimal care to improve the patient's functional independence and quality of life. The conditions associated with HIV infection are insidious, slow, and crushing in nature. The medical community can help the patient with HIV infection and AIDS remain on his or her feet. By doing this, costs, both social and economic, can be lowered. The podiatrist must have a strong knowledge of the pathology of AIDS. He or she must use PT along with other disciplines: podiatric medicine, orthotic therapy, and general podiatric care. PT is effective in treating conditions of the lower extremities that affect the CNS, PNS, musculoskeletal system, and, lastly, rheumatologic effects of HIV infection.

The in vitro inhibition of insulin released by alloxan (20 mg/100 ml) in collagenase isolated rat islets is preferentially prevented by alpha D-glucose at a concentration of 1.0 mg/ml, while at a higher anomer concentration (1.5 mg/ml) both alpha and beta D-glucose provide equal protection. The ability of alpha D-glucose compared with beta D-glucose to stimulate insulin release, in vitro, showed a similar dose-related response, as observed in the alloxan protective studies. Although, both alpha and beta D-glucose compete with mutorated D-glucose for transport into islet cells, neither anomer produced a significantly different degree of inhibition in the transport process. The shared alpha stereospecificity for D-glucose in protection against alloxan and in stimulating insulin secretion in these in vitro studies, suggest a common site of interaction which may involve the beta-cell membrane.

In the present study, a colchicine binding assay was used to measure changes in islet polymerized and depolymerized tubulin at intervals characterizing the biphasic pattern of glucose-induced insulin release i.e., 2.5, 5.5, 10.5, and 30.5 min. At 2.5 min during the rapid onset of insulin release, a significant increase from 24% to 33% in polymerized tubulin content was observed. This increase in polymerized tubulin was followed by a reduction that temporally correlated with the disappearance of first phase release. Second phase release was also associated with a shift in equilibrium favoring tubulin polymerization at longer incubation periods. The effect of cytochalasin B on the equilibrium between polymerized and depolymerized tubulin was evaluated at a submaximal glucose concentration of 16.5 mM. Under these conditions, cytochalasin B increased polymerized tubulin content in a manner that parallels its enhancing effect on insulin release. These results indicate that the rapid events associated with the biphasic pattern of insulin release are temporally correlated with changes in polymerized tubulin.

Isloated rat islets were maintained in vitro in a perifusion system, exposed to alloxan (20 mg/100 ml) for 5 minutes in the presence of agents which affect cAMP metabolism and subsequently stimulated with glucose. The rate of insulin secretion was monitored throughout the period of perifusion. Exposure to alloxan alone produces complete inhibition of glucose-induced insulin release [18] whereas concomitant exposure to carreine and theophylline for this brief interval provided almost complete protection of the islets from the inhibitory action of alloxan. Glucagon, cAMP and CBcAMP did not protect the islets form alloxan. Pre-treatment of the islets with either theophylline or glucagon and DBcAMP did not provide protection. These findings indicate that the protective action of theophylline and carreine against alloxan is unrelated to the effect of these agents on cAMP metabolism in the beta cell.

The uptake of theophylline and caffeine was determined in isolated pancreatic islets employing a dual isotope procedure with sucrose as an extracellular marker. Islets rapidly accumulated caffeine and theophylline with apparent dissociation constants of approximately 23 and 6 mM, respectively. Theophylline inhibited the uptake of caffeine and caused displacement of caffeine from islets. These results indicated a competition by theophylline and caffeine for a common site (binding and/or transport carrier). In addition, theophylline and caffeine inhibited D-glucose transport in a dose-dependent manner and within the limits of the experimental system, this inhibition appeared to be non-competitive. (Bu)2cAMP under similar experimental conditions exerted no effect on D-glucose transport. These results present evidence for a rapid uptake of theophylline and caffeine in pancreatic islets, which is compatible with their immediate cellular effects. In addition, these results demonstrate a direct effect by theophy...

Ninhydrin (85 /XM), a stable analog of alloxan, inhibited insulin release in a time-dependent manner. When Dglucose was present immediately after brief exposures of 1-2 min, part of the subsequent inhibition by ninhydrin was prevented. Ninhydrin inhibition of glucose-induced insulin release was not mediated by inhibition of the facilitated transport of Dglucose. These findings are identical to the in vitro interactions of alloxan with the insulin release mechanism and suggest that alloxan and ninhydrin inhibit secretion by a similar mechanism. The uptake of [3H]ninhydrin was measured in isolated islets and shown to be rapidly accumulated. The common interaction between alloxan and ninhydrin was further supported by the ability of alloxan pretreatment to alter the subsequent islet content of [3H]ninhydrin. D-Glucose decreased the islet content of label derived from ['H]ninhydrin under conditions which prevented ninhydrin inhibition of insulin release. The testagents, 3-O-methyl-D-glucose, caffeine, and L-g...

Active calcium uptake was demonstrated in a subcellular fraction of islets which was enriched in endoplasmic reticulum. Calcium uptake was stimulated by ATP in a magnesium-dependent manner. The rate of calcium accumulation was sustained by oxalate (10 mM) and uptake was prevented or reversed by addition of the calcium ionophore A23187. This calcium uptake process was not affected by azide or ruthenium red. Direct comparison of calcium uptake by endoplasmic reticulum-enriched and plasma membrane-enriched fractions indicated that the uptake was not due to contamination of the fraction with plasma membrane vesicles. These factors as well as the purity of the fraction indicate that the calcium uptake system resides in the endoplasmic reticulum. The properties of the islet endoplasmic reticulum calcium uptake system are similar to properties reported for endoplasmic reticulum derived from other cell types. These properties include stimulation by potassium and a Km for ionized calcium of 1.5 +/- 0.3 microM. The islet-cell endoplasmic reticulum may play a critical role in cellular calcium homeostasis and contribute to the regulation of insulin secretion.

Ninhydrin, a compound which shares chemical properties strikingly similar to alloxan was found to mimic basically the inhibitory effect of alloxan on glucose-induced insulin release. Exposure of pancreatic islets for five minutes to 85 mumol/l ninhydrin produced approximately ninety percent inhibition of subsequent glucose-induced insulin release without altering basal secretion. Both D-glucose and D-mannose provided substantial protection against the inhibitory effect of ninhydrin, and the alpha anomer of D-glucose was more effective than the beta anomer in preventing ninhydrin inhibition of insulin release. Evidence for a common site of inhibition by ninhydrin and alloxan in the insulin release process is discussed.

Active calcium uptake was demonstrated in a subcellular fraction of islets which was enriched in endoplasmic reticulum. Calcium uptake was stimulated by ATP in a magnesium-dependent manner. The rate of calcium accumulation was sustained by oxalate (10 mM) and uptake was prevented or reversed by addition of the calcium ionophore A23187. This calcium uptake process was not affected by azide or ruthenium red. Direct comparison of calcium uptake by endoplasmic reticulum-enriched and plasma membrane-enriched fractions indicated that the uptake was not due to contamination of the fraction with plasma membrane vesicles. These factors as well as the purity of the fraction indicate that the calcium uptake system resides in the endoplasmic reticulum. The properties of the islet endoplasmic reticulum calcium uptake system are similar to properties reported for endoplasmic reticulum derived from other cell types. These properties include stimulation by potassium and a Km for ionized calcium of 1.5 +/- 0.3 microM. The islet-cell endoplasmic reticulum may play a critical role in cellular calcium homeostasis and contribute to the regulation of insulin secretion.

The uptake of theophylline and caffeine was determined in isolated pancreatic islets employing a dual isotope procedure with sucrose as an extracellular marker. Islets rapidly accumulated caffeine and theophylline with apparent dissociation constants of approximately 23 and 6 mM, respectively. Theophylline inhibited the uptake of caffeine and caused displacement of caffein from islets. These results indicated a competition by theophylline and caffeine for a common site (binding and/or transport carrier). In addition, theophylline and caffeine inhibited D-glucose transport in a dose-dependent manner and within the limits of the experimental system, this inhibition appeared to be non-competitive. (Bu)2cAMP under similar experimental conditions exerted no effect on D-glucose transport. These results present evidence for a rapid uptake of theophylline and caffeine in pancreatic islets, which is compatible with their immediate cellular effects. In addition, these results demonstrate a direct effect by theophylline and caffeine on D-glucose transport which appears independent of their ability to alter intracellular cAMP levels.

The effect of cytochalasin B on the biphasic pattern of insulin secretion was studied. Islets were isolated from the normal rat pancreas by the collagenase technique and maintained in vitro by perifusion. Cytochalasin B produced a significant increase in the rate of insulin secretion in the first and second phase of glucose-induced insulin release and enhanced significantly the monophasic pattern of release induced by tolbutamide. The drug had no effect on insulin release in the presence of non—stimulatory levels of glucose. The enhancing effect on glucose—induced insulin secretion required the continued presence of cytochalasin B. Removal of the drug during the second phase of glucose—induced insulin secretion resulted in a rapid decline in the rate of insulin release. Islets were perifused with glucose, glucagon and theophylline in order to obtain maximal stimulation of insulin release. Under these conditions of marked stimulation, cytochalasin B did not produce a further significant enhancement of insu...

A simple perifusion system for in vitro studies on the rate of insulin secretion of isolated rat islets is described. A biphasic pattern of insulin secretion was produced by glucose whereas tolbutamide stimulated only the first phase of insulin secretion. The perifusion system was used to determine the effect of anti-mitotic agents on the biphasic pattern of insulin secretion. Yinblastine and colchicine destroy microtubules whereas deuterium oxide (D2O) produces stabilization and interference with the function of microtubules. Vinblastine (10-4 M) and D2O (100 per cent) inhibited completely the first and second phase of glucose-induced insulin secretion. The inhibitory effect of D2O was reversible and a biphasic pattern of secretion occurred following the replacement of D2O with water. Colchicine (10-3 M) produced significant inhibition of only the second phase of glucose-induced insulin secretion. The first phase of tolbutamide-induced insulin secretion was inhibited by vinblastine and D2O and the inhibitory effect of D2O was reversible. Colchicine did not inhibit the first phase of tolbutamide-induced insulin release. These findings indicate that the microtubular system is involved in both phases of insulin secretion. The first phase of secretion may be due to the release of beta granules already associated with the microtubular system and the second phase could be the result of stored and newlysynthesized granules becoming associated with the system.